scholarly journals Murine Neonates Infected with Yersinia enterocolitica Develop Rapid and Robust Proinflammatory Responses in Intestinal Lymphoid Tissues

2013 ◽  
Vol 82 (2) ◽  
pp. 762-772 ◽  
Author(s):  
David T. Siefker ◽  
Andrea Echeverry ◽  
Roberta Brambilla ◽  
Masayuki Fukata ◽  
Kurt Schesser ◽  
...  
Keyword(s):  
Gene Expression ◽  
Yersinia Enterocolitica ◽  
Lymphoid Tissues ◽  
Virulence Plasmid ◽  
Wild Type ◽  
Mesenteric Lymph Nodes ◽  
Content Type ◽  
Proinflammatory Responses ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

ABSTRACTNeonatal animals are generally very susceptible to infection with bacterial pathogens. However, we recently reported that neonatal mice are highly resistant to orogastric infection withYersinia enterocolitica. Here, we show that proinflammatory responses greatly exceeding those in adults arise very rapidly in the mesenteric lymph nodes (MLN) of neonates. High-level induction of proinflammatory gene expression occurred in the neonatal MLN as early as 18 h postinfection. Marked innate phagocyte recruitment was subsequently detected at 24 h postinfection. Enzyme-linked immunosorbent spot assay (ELISPOT) analyses indicated that enhanced inflammation in neonatal MLN is contributed to, in part, by an increased frequency of proinflammatory cytokine-secreting cells. Moreover, both CD11b+and CD11b−cell populations appeared to play a role in proinflammatory gene expression. The level of inflammation in neonatal MLN was also dependent on key bacterial components.Y. enterocoliticalacking the virulence plasmid failed to induce innate phagocyte recruitment. In contrast, tumor necrosis factor alpha (TNF-α) protein expression and neutrophil recruitment were strikingly higher in neonatal MLN after infection with ayopP-deficient strain than with wild-typeY. enterocolitica, whereas only modest increases occurred in adults. This hyperinflammatory response was associated with greater colonization of the spleen and higher mortality in neonates, while there was no difference in mortality among adults. This model highlights the dynamic levels of inflammation in the intestinal lymphoid tissues and reveals the protective (wild-type strain) versus harmful (yopP-deficient strain) consequences of inflammation in neonates. Moreover, these results reveal that the neonatal intestinal lymphoid tissues have great potential to rapidly mobilize innate components in response to infection with bacterial enteropathogens.

scholarly journals Yersinia pseudotuberculosis Efficiently Escapes Polymorphonuclear Neutrophils during Early Infection

2013 ◽  
Vol 82 (3) ◽  
pp. 1181-1191 ◽  
Author(s):  
Linda Westermark ◽  
Anna Fahlgren ◽  
Maria Fällman
Keyword(s):  
Dendritic Cells ◽  
Yersinia Pseudotuberculosis ◽  
Immune Defense ◽  
Polymorphonuclear Neutrophils ◽  
Lymphoid Tissues ◽  
Wild Type ◽  
Mesenteric Lymph Nodes ◽  
Content Type ◽  
Effective Dissemination

ABSTRACTThe human-pathogenic species of the Gram-negative genusYersiniapreferentially target and inactivate cells of the innate immune defense, suggesting that this is a critical step by which these bacteria avoid elimination and cause disease. In this study, bacterial interactions with dendritic cells, macrophages, and polymorphonuclear neutrophils (PMNs) in intestinal lymphoid tissues during earlyYersinia pseudotuberculosisinfection were analyzed. Wild-type bacteria were shown to interact mainly with dendritic cells, but not with PMNs, on day 1 postinfection, while avirulentyopHandyopEmutants interacted with PMNs as well as with dendritic cells. To unravel the role of PMNs during the early phase of infection, we depleted mice of PMNs by using an anti-Ly6G antibody, after which we could see more-efficient initial colonization by the wild-type strain as well as byyopH,yopE, andyopKmutants on day 1 postinfection. Dissemination ofyopH,yopE, andyopKmutants from the intestinal compartments to mesenteric lymph nodes was faster in PMN-depleted mice than in undepleted mice, emphasizing the importance of effective targeting of PMNs by theseYersiniaouter proteins (Yops). In conclusion, escape from interaction with PMNs due to the action of YopH, YopE, and YopK is a key feature of pathogenicYersiniaspecies that allows colonization and effective dissemination.

Abstract 563: Oxidized LDL Promotes Endothelial NF-kappaB Activation and Inflammation Through Focal Adhesion Kinase-dependent RSK Signaling

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Arif Yurdagul ◽  
Christopher B Pattillo ◽  
David D Schlaepfer ◽  
Wayne Orr
Keyword(s):  
Gene Expression ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Oxidized Ldl ◽  
Monocyte Adhesion ◽  
Proinflammatory Responses ◽  
Proinflammatory Gene ◽  
Ribosomal S6 Kinase ◽  
Nf Kappab ◽  
Proinflammatory Gene Expression

Oxidized LDL (oxLDL) accumulates early in atherosclerosis and promotes endothelial NF-kappaB activation, proinflammatory gene expression, and monocyte adhesion. Like other atherogenic factors, oxLDL-induced proinflammatory responses requires integrin-dependent focal adhesion kinase (FAK) signaling; however, the mechanism by which FAK mediates oxLDL-dependent NF-kappaB signaling has yet to be revealed. We now show that oxLDL induces NF-kappaB activation and VCAM-1 expression through FAK-dependent IkappaB kinase beta (IKKbeta) activation. We further identify FAK-dependent activation of p90 ribosomal S6-kinase (RSK) as a critical mediator of oxLDL-dependent IKKbeta/NF-kappaB signaling, as inhibiting RSK blocks oxLDL-induced IKKbeta/NF-kappaB activation, VCAM-1 expression, and monocyte adhesion. Lastly, transgenic mice containing a kinase-dead mutation in FAK specifically in the endothelial cells show reduced RSK activity, decreased VCAM-1 expression, and reduced macrophage accumulation in regions of early atherosclerosis. Taken together, our data elucidates a novel mechanism whereby oxLDL-induced endothelial FAK signaling drives an ERK/RSK pathway to activate IKKbeta/NF-kappaB signaling and proinflammatory gene expression.

scholarly journals Effects of Saline, an Ambient Acidic Environment, and Sodium Salicylate on OXA-Mediated Carbapenem Resistance in Acinetobacter baumannii: TABLE 1

2016 ◽  
Vol 60 (6) ◽  
pp. 3415-3418 ◽  
Author(s):  
Esther Zander ◽  
Harald Seifert ◽  
Paul G. Higgins
Keyword(s):  
Gene Expression ◽  
Acinetobacter Baumannii ◽  
Sodium Salicylate ◽  
Carbapenem Resistance ◽  
Low Ph ◽  
Wild Type ◽  
Experimental Conditions ◽  
Content Type ◽  
Reference Strains

Different physiological conditions, such as NaCl, low pH, and sodium salicylate, have been shown to affect antibiotic resistance determinants inAcinetobacter baumanniiisolates. Therefore, the aim of this study was to investigate the effects of NaCl, sodium salicylate, and low pH on the susceptibility ofA. baumanniito carbapenem. We cloned genes encoding oxacillinases (OXA) of different subclasses, with their associated promoters, from carbapenem-resistantA. baumanniiisolates into the same vector and transferred them to theA. baumanniireference strains ATCC 19606 and ATCC 17978. Carbapenem MICs were determined at least in triplicate by agar dilution under standard conditions, as well as in the presence of 200 mM NaCl or 16 mM sodium salicylate, or at pH 5.8. OXA-58-like gene expression was determined by reverse transcription-quantitative PCR (qRT-PCR). Under some experimental conditions, significant MIC reductions were shown for some transformants but not for others. Only in one instance were all transformants harboring the same OXA affected by the same condition: at pH 5.8, the imipenem and meropenem MICs for strains expressing OXA-58-like enzymes decreased from a resistant level (32 to 64 mg/liter) to an intermediate-susceptible level (8 mg/liter). However,blaOXA-58-likegene expression remained the same. MICs for both wild-type reference strains were not affected by the conditions tested. Our results indicate that the effects of the experimental conditions tested on OXAin vivoare mostly strain dependent. MICs were not reduced to wild-type levels, suggesting that the conditions tested do not lead to complete OXA inhibition in the bacterial cell.

CCAAT/enhancer binding protein δ regulates glial proinflammatory gene expression

2013 ◽  
Vol 34 (9) ◽  
pp. 2110-2124 ◽  
Author(s):  
Tony Valente ◽  
Marco Straccia ◽  
Nuria Gresa-Arribas ◽  
Guido Dentesano ◽  
Josep M. Tusell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression

scholarly journals Temporal Transcriptomics of Gut Escherichia coli in Caenorhabditis elegans Models of Aging

2021 ◽  
Author(s):  
Joshua D. Brycki ◽  
Jeremy R. Chen See ◽  
Gillian R. Letson ◽  
Cade S. Emlet ◽  
Lavinia V. Unverdorben ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Health Span ◽  
Content Type ◽  
C Elegans ◽  
Evolutionarily Conserved

Previous research has reported effects of the microbiome on health span and life span of Caenorhabditis elegans , including interactions with evolutionarily conserved pathways in humans. We build on this literature by reporting the gene expression of Escherichia coli OP50 in wild-type (N2) and three long-lived mutants of C. elegans .

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